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The effect of a hormone is amplified as the signaling pathway progresses. The binding of a hormone at a single receptor causes the activation of many G-proteins, which activates adenylyl cyclase. Each molecule of adenylyl cyclase then triggers the formation of many molecules of cAMP. Further amplification occurs as protein kinases, once activated by cAMP, can catalyze many reactions. In this way, a small amount of hormone can trigger the formation of a large amount of cellular product. To stop hormone activity, cAMP is deactivated by the cytoplasmic enzyme phosphodiesterase, or PDE. PDE is always present in the cell, breaking down cAMP to control hormone activity; thus, preventing overproduction of cellular products.
The mechanism of action of steroid hormones involves their interaction with tissue-specific binding sites, and results in a precise modulation of gene expression. Both high-affinity receptors and secondary binding sites exist for steroid hormones in target tissues. Only steroid-receptor complexes were, in several cases, clearly shown to directly regulate transcription by interacting with DNA region(s) close to steroid-controlled genes. However other indications suggest that steroid hormones could also modulate transcription by altering chromatin conformation. These modifications encompass post-traductional modifications of histones and non-histone proteins, as well as changes in the pattern of histone variants. Beside transcription, there are also evidences that steroid hormones can modulate gene expression by regulating some RNA processing events. Whether high-affinity receptors or secondary binding sites directly regulate these events is not known. These observations however suggest that several levels of control might exist for steroid hormones to precisely regulate gene expression.